分类目录归档：Sciencenews

Researchers provide updated fossil hominin body mass estimates

Date:

August 3, 2015

Source:

George Washington University

Summary:

A new analysis of early hominin body size evolution suggests that the earliest members of the Homo genus (which includes our species, Homo sapiens) may not have been larger than earlier hominin species.

Researchers provide the most comprehensive set of body mass estimates, species averages and species averages by sex for fossil hominins to date (stock image).

A new analysis of early hominin body size evolution led by a George Washington University professor suggests that the earliest members of the Homogenus (which includes our species, Homo sapiens) may not have been larger than earlier hominin species. As almost all of the hows and whys of human evolution are tied to estimates of body size at particular points in time, these results challenge numerous adaptive hypotheses based around the idea that the origins of Homo coincided with, or were driven by, an increase in body mass.

In “Body Mass Estimates of Hominin Fossils and the Evolution of Human Body Size,” published online in the Journal of Human Evolution, Mark Grabowski assistant research professor in the GW Center for the Advanced Study of Human Paleobiology, and his co-authors provide the most comprehensive set of body mass estimates, species averages and species averages by sex for fossil hominins to date. Produced using cutting-edge methodology and the largest sample of individual early hominin fossils available, analysis of their results shows that early hominins were generally smaller than previously thought and that the increase in body size occurred not between australopiths and the origins of Homo but later with H. erectus(the first species widely found outside of Africa).

“One of our major results is that we found no evidence that the earliest members of our genus differed in body mass from earlier australopiths (some of the earliest species of hominins),” said Dr. Grabowski, who is also a Fulbright scholar at the Centre for Ecological and Evolutionary Synthesis at the University of Oslo. “In other words, the factors that set our lineage apart from our earlier ancestors were unrelated to an increase in body size, which has been the linchpin of numerous adaptive hypotheses on the origins of our genus.”

“There are several untested assumptions about the origin of Homo,” said Bernard Wood, University Professor of Human Origins at GW, who was not an author on the study. “This study debunks the one that suggests that until the origin of our own genus, for one reason or another — and the usual explanation is not enough meat in the diet — all early hominins were small-bodied. This elegant study shows that body size did not make a sharp uptick with the arrival of early Homo. My prediction is that this is just the first of many preconceptions about early Homo that will be debunked in the next few years.”

Until now, anthropologists have generally relied on estimates of hominin body mass presented in a paper by Henry M. McHenry in 1992. Since then, many more fossils have been discovered and researchers better understand the complexities of human evolution. Dr. Grabowski and his co-authors build on and update McHenry’s results and apply new and novel methods to analyze a comprehensive fossil data set. The researchers hope their results will be the new standard for fossil hominin body estimates.

In addition, Dr. Grabowski and the co-authors found that the level of size difference between males and females (sexual dimorphism) appears to have only slightly decreased from earlier hominin species by the time of early H. erectus, and only decreased to modern human-like low levels later in our lineage. High levels of dimorphism such as in gorillas may correlate with more “harem”-like social structures. This result should give pause to evolutionary models that see a more modern human-like monogamous social structure evolving early in our lineage.

An analysis of data on stomach acidity and diet in birds and mammals suggests that high levels of stomach acidity developed not to help animals break down food, but to defend animals against food poisoning. The work raises interesting questions about the evolution of stomach acidity in humans, and how modern life may be affecting both our stomach acidity and the microbial communities that live in our guts.

Hooded vulture eating (stock image). The researchers found that scavengers, or species that eat food at high risk of microbial contamination, have more acidic stomachs. This acidity allows the stomach to act as a filter, effectively controlling which microbes can pass through the stomach to the gut.

An analysis of data on stomach acidity and diet in birds and mammals suggests that high levels of stomach acidity developed not to help animals break down food, but to defend animals against food poisoning. The work raises interesting questions about the evolution of stomach acidity in humans, and how modern life may be affecting both our stomach acidity and the microbial communities that live in our guts.

“We started this project because we wanted to better understand the relationship between stomach acidity, diet and the microbes that live in the guts of birds and mammals,” says DeAnna Beasley, a postdoctoral researcher at North Carolina State University and corresponding author of a paper on the work. “Our idea was that this could offer some context for looking at the role of the human stomach in influencing gut microbes, and what that may mean for human health.”

The research team — including scientists from Washington University and the University of Colorado, Boulder — examined all of the existing literature on stomach acidity in birds and mammals, and found data on 68 species. They then collected data on the natural feeding habits of each species. The researchers then ran an analysis to see how feeding behavior was related to stomach acidity.

The researchers found that scavengers, or species that eat food at high risk of microbial contamination, have more acidic stomachs. This acidity allows the stomach to act as a filter, effectively controlling which microbes can pass through the stomach to the gut.

“The finding confirms our hypothesis, but you have to get that confirmation before moving forward,” Beasley says. “The next step will be for scientists to examine the microbial ecosystems in the guts of these animals to see how these ecosystems have evolved. Do animals with high stomach acidity have smaller or less diverse populations of gut microbes? Or do they simply host microbes that can survive in acidic environments?”

One surprise was that, while the researchers classified humans as omnivores, human stomachs have the high acidity levels normally associated with scavengers. Meanwhile, the literature shows that medical treatments — from surgery to antacids — can significantly alter the acidity in a human stomach.

“This raises significant questions about how humans have evolved, our species’ relationship with food over time, and how modern changes in diet and medicine are affecting our stomachs, our gut microbes and — ultimately — our health,” Beasley says. “Those are questions the research community is already exploring, and the answers should be interesting.”

By recreating the firefly’s glow in the lab, scientists continue to tease out the secrets behind how the insects light up, the American Chemical Society announced in a new video. Scientists had known that a compound called luciferase produced the firefly’s glow. Now, a new study published in the Journal of the American Chemical Societydescribes how a molecule toxic to most animals, called a superoxide ion, plays a key role in the reactions that cause luciferase to produce light. Superoxide, which can cause inflammation and cell damage in humans and other animals, doesn’t appear to harm the bug because the reactions are contained and happen quickly, the scientists say. The finding could lead to important applications in medicine, especially in cancer research where luciferase’s light can be used to track how a tumor spreads through an organism.

One terrifying bug has been helping scientists bring the endangered Iberian lynx back from the edge of extinction,Discover reports. Scientists used the insect, known as the triatomine assassin bug, to collect blood samples from the wildcats. Because of stress and inexperience, female lynxes new to pregnancy often lose their first litter. Scientists, who wanted to prevent that from happening, needed the blood samples to identify when a pregnancy had occurred. But they feared that tranquilizing the animals in order to collect the samples would itself cause distress. To avoid that, the scientists employed the bug and its hollow, needlelike mouthpart. Although useful, the bug’s time as a syringe was limited; today the scientists use a fecal pregnancy test.

Seabirds called shearwaters manage to navigate across long stretches of open water to islands where the birds breed. It’s not been clear how the birds do this, but there have been some clues. When scientists magnetically disturbed Cory’s shearwaters, the birds still managed to find their way. But when deprived of their sense of smell, the shearwaters had trouble homing in on their final destination.

Smell wouldn’t seem to be all that useful out over the ocean, especially with winds and other atmospheric disturbances playing havoc on any scents wafting through the air. But now researchers say they have more evidence that shearwaters are using olfactory cues to navigate. Andrew Reynolds of Rothamsted Research in Harpenden, England, and colleagues make their case June 30 in theProceedings of the Royal Society B.

Messing with Cory’s shearwaters or other seabirds, like researchers did in earlier studies, wasn’t a good option, the researchers say, because there are conservation concerns when it comes to these species. Instead, they attached tiny GPS loggers to 210 shearwaters belonging to three species: Cory’s shearwaters, Scopoli’s shearwaters and Cape Verde shearwaters.

But how would the birds’ path reveal how they were navigating? If they were using olfactory cues, the team reasoned, the birds wouldn’t take a straight path to their target. Instead, they would fly straight for a time, guided in that direction by a particular smell. When they lost that scent, their direction would change, until they picked up another scent that could guide them. And only when a bird got close would it use landmarks, other birds and the odor of the breeding colony as guides. If the birds were using some other method of navigation — or randomly searching for where to go — their paths would look much different.

When the researchers analyzed the paths of the shearwaters, 69 percent of the birds moved in a way that matched what was expected if they were using olfactory cues. Nearly all of the journeys that lasted four or more days took this kind of path, but less than half of short flights that lasted less than two days had this kind of flight path.

“All these animals share the same basic pattern,” the researchers write, “strongly suggesting the presence of an underlying common mechanism of orientation which we have identified as olfactory-cued navigation.”

Influenza viruses evolve constantly, but so does flu science

You go to bed feeling fine. The next morning you’re sick with a fever, exhaustion, headache, body aches and more.

You may have influenza, better known as the flu. It’s caused by a virus, a tiny bit of genetic material surrounded by a protein. Flu viruses infect the nose, throat and lungs. (If people claim to have “stomach flu,” they are mistaken. They really have some other infection.)

Every year, between 5 percent and 20 percent of all Americans come down with the flu. Those numbers come from the U.S. Department of Health and Human Services in Washington, D.C. Complications send more than 200,000 of these flu victims to the hospital each year. Worse, the flu kills anywhere from 3,000 to 49,000 people annually — and that’s just in the United States.

A widespread outbreak of flu or another infectious disease is called an epidemic. In some years, flu spreads so far and so fast that it causes a worldwide epidemic. This is known as a pandemic. Researchers hope to prevent a pandemic if possible. One tactic: vaccines.

Flu vaccines offer people some immunity. Immunity is the body’s ability to resist a particular disease by making proteins called antibodies. A vaccine can give that process a head start. However, no vaccine yet can fight all types, or strains, of flu.

What’s more, notes David Morens, “Flu is not one virus. It’s many, many viruses.” Morens works at the National Institutes of Health in Bethesda, Md. As an epidemiologist, he studies the causes, patterns and effects of disease in populations.

Flu viruses constantly evolve. That means their genes undergo change. Those changes are called mutations. And some mutations can let a virus evade any immunity, says Morens. Each year, the flu vaccine is updated to keep up with those mutations. The vaccine targets strains based on what health experts saw happening with different strains the previous flu season.

Recently, an usually high percentage of changes happened in one type of flu virus, known as H3N2. As a result, the vaccine for the 2014 to 2015 flu season didn’t work well. In fact, the vaccine was only about one-third as effective as a well-matched vaccine would have been. Scientists from the Centers for Disease Control and Prevention and other organizations reported the results this past January 16 in Morbidity and Mortality Weekly Report.

Recently, health officials decided the vaccine for the upcoming flu season in the United States will include the H3N2 “Switzerland” type that made this year’s vaccine a poor match. It will have a new “Type B” strain as well. But new mutations keep occurring. Vaccines are “always a little behind,” Morens notes.

Now science aims to get ahead of the flu. Some researchers are trying to gauge how flu evolves. These experts want to know what strains are likely to strike hard and soon. Others are searching for vulnerabilities common to all types of flu. Still other scientists are looking for ways to stop new flu strains before they can easily infect people at all.

Constantly evolving

Katia Koelle is a biologist at Duke University in Durham, N.C. She says that one reason researchers have trouble keeping up with new flu types is the fact that these infections are caused by an RNA virus. RNA is short for ribonucleic (RY-boh-nu-KLAY-ic) acid. Cells grow and act by making specific chemicals called proteins. Cells do so at the right time and the right place with a type of RNA.

Like that RNA, a flu virus has a single strand of genetic material. Once in host cells, the virus gets the cell to copy its genetic code over and over to make more virus.

But “mutations arise all the time in flu,” Koelle notes. Here is one big reason: RNA viruses “don’t have proofreading mechanisms.” So they don’t detect a mistake and correct or eliminate mistakes that copying errors introduce. If the error doesn’t kill the virus, the affected RNA will show up in future generations. Such errors will get copied over and over whenever the virus reproduces. It’s like a printing press spitting out thousands of newspapers with the same misspelled headline.

That’s different from DNA viruses, a family that includes the one that causes chickenpox. When DNA reproduces, each bit on its double strands can partner only with a specific part on the other. It’s like a zipper. Each half has to pair with the other half. If there’s a snag, the process stops. Without that check, RNA viruses can get “sloppy,” Koelle says.

Researchers want better ways to predict which flu strains will hit people hardest next year. To do that, researchers at the University of Cologne in Germany and Columbia University in New York City have made a computer model. This computer program has equations, program instructions and data for thousands of strains of H3N2 (a common flu type).

The team focused on the gene for a protein found on the surface of the flu virus. That protein ishemagglutinin, or HA. HA helps the flu virus hook onto host cells. Antibodies can prevent HA’s action. But those antibodies work only if they can latch onto HA just right. Think of it as a matching lock and key set.

The researchers asked the computer model to sift through and find those strains least likely to encounter matching antibody “keys.” If few antibodies could lock up these virus strains, most people would be at risk of becoming infected by them.

“Basically, the rarer it’s been in the past, the better” a flu strain will do, says Koelle. She reviewed this study that used computer modeling before Nature published it in March. If new vaccines targeted those strains, the vaccines would equip more people with effective antibodies. Fewer people should then get sick from those strains.

Of course, new flu strains will still evolve. But the hope is that each year’s modeling will flag them early.

How viruses morph

Koelle also uses computer modeling to study how viruses evolve. Some mistakes in copying the RNA code can doom a virus. But about 8 percent to 10 percent of those RNA changes help the virus survive, she says. These survivors might then infect more people.

Other RNA changes are what Koelle calls “garbage” mutations. They don’t kill the virus. Still, these mutations can make the virus less likely to survive and reproduce. About 40 percent of mutations in RNA viruses fall into that “harmful” category, she says.

One of Koelle’s projects looks at links between “garbage” mutations and other mutations that give flu strains an edge. Remember that when the flu virus reproduces, all its genetic code gets copied, unless more mutations occur. Thus, an RNA change that helps a flu virus survive and spread means there will be more reproduction of its genetic code, including any “garbage” mutations. Koelle says it’s as if a bad student copies someone’s homework. That student will aim to copy everything, including both right and wrong answers.

Even though the “garbage” mutations carry forward into future generations, they might still “shape some patterns of evolution,” Koelle notes. For example, these changes might affect the rate of future mutations. Or the changes might affect where and how a virus spreads among people. Ideally, understanding the “garbage” could lead to new ways to fight flu.

Another computer-modeling project focuses on changes that might help the virus more quickly find host cells. “Once it’s in the host cell, an antibody can’t get it,” Koelle explains. Getting into host cells more quickly thus lets a virus strain “run and hide faster” from antibodies, she says. Computer modeling with data from work by other researchers could give clues about how those mutations work. Knowing that could help researchers figure out better ways to defeat the viruses with vaccines.

Universal solutions?

Viruses can’t reproduce by themselves. Instead, they must invade the cells of another organism. Once inside, a virus turns the cells of its host into virus factories. Researchers are using another computer model to look at how that process starts. It focuses on the steps the HA protein goes through as it attaches to the outside of a new host cell.

“From experiments, we know that HA folds into two different structures— one before it connects [with a host cell] and one after,” explains Jeffrey Noel. He’s a biological physicist at Rice University in Houston, Texas. Noel and his team created a computer model that uses physics principles to figure out how the refolding happens.

Before it latches onto a host cell, the HA protein can have any of several shapes. Again, some of those variations can keep antibodies from working. As noted before, the protein and antibodies must fit like a lock and key.

Meanwhile, the inner part of the HA protein pretty much stays the same from one type of flu virus to the next. “The virus can’t mutate that part of the protein very much,” Noel says. And it’s that inner part of the protein that lets the virus invade the cell.

As HA refolds, the protein exposes that inner part. Experts see this as a vulnerability. That exposure might be a chance “to go inside the fence and attack” the protein with a medicine, notes Noel. And since that part of the protein generally doesn’t change, such a medicine might work against many types of flu, he says. His team published its findings in the August 19, 2014, issue of the Proceedings of the National Academy of Sciences.

Still other research asks basic science questions about “what flu viruses do and how they do it,” notes Morens. For example, ducks and other birds naturally harbor flu viruses (often with no sign of disease). “How does a bird virus get to be a human virus?” he asks.

Changes that let flu viruses move from another species into humans are relatively rare. Yet those rare mutations pose big threats. When transfers happen, no one will have immunity for quite a while. If a new strain spreads very quickly among people, it risks becoming a pandemic.

Flu’s migrations

Flu doesn’t just move from birds to humans. Bird flu also can go to pigs or other mammals. Scientists at St. Jude Children’s Research Hospital in Memphis, Tenn., and other organizations found one form had infected harbor seals in 2011. That strain most likely came from a wild sea bird, notes Stacey Schultz-Cherry. She’s a virologist at the Memphis hospital.

Viruses infect animal cells by binding to sugars on their surface,

or membrane, Schultz-Cherry explains. “These bird viruses typically can’t get into the cells” of mammals. That is because birds and mammals have different sugars on their membranes.

Schultz-Cherry compares it to trying to pick out someone in a crowd. If you’re told to “look for a guy in a yellow raincoat,” you know whom to look for. That is true even if you haven’t met the person before.

In this case, though, the bird virus changed. It found a way to recognize the sugar on seal cells. Nature Communications reported her team’s findings on September 3, 2014.

“No human illness was linked to the 2011 harbor seal virus,” Schultz-Cherry says. However, scientists think infected seals did transmit flu to people in the 1880s. And flu can indeed pass into people from other types of mammals. Flu also can go from people into other mammals — and maybe even back again. A study in the August 2014 Journal of Virology showed that human flu can infect dogs, for example.

“There must be some kind of host-switching process,” Morens says. But right now, “we have no idea how that happens.”

For one thing, genetically, bird viruses look very different from human viruses. Also, a virus can’t survive long outside a cell. Scientists are now scouting for various in-between hosts. But with so many strains and mutations, finding a host-jumping virus can be like looking for a needle in a haystack.

Lab studies can explore, in a more orderly way, how flu viruses evolve. Some studies start with a bird flu virus and work forward. Researchers alter the virus’s genetic code and see whether the change lets the virus infect a mammal, such as a ferret.

Other lab studies work backward. Suppose your research team finds 100 differences between a human virus and the bird virus that was its likely source. “Then you start one by one getting rid of each mutation and see what happens,” says Morens. How does each change to the virus affect its ability to infect human cells?

Repeating the process over and over could show steps in the host-jumping process. “We want to know what those steps are,” says Morens. That will provide a general picture “of how the evolution occurred.”

Once scientists know that, they might find a way to stop the process before people get sick. Meanwhile, other researchers continue the search for better vaccines. Perhaps you might help make some of these important discoveries. “We desperately need more people in science,” says Schultz-Cherry.

In the meantime, good health habits can cut our risk of becoming infected. “Wash your hands,” Schultz-Cherry recommends. And get your flu shot, she adds. Tell your family members to do the same. Eat healthy foods and get enough sleep too. These are ways all of us can help fight the flu.

Roll over Beethoven and tell Tchaikovsky the news: Scientists have for the first time identified key characteristics of music worldwide. The findings lay the groundwork for deciphering why people everywhere sing, play instruments and find melodies so compelling.

No musical features, not even simple scales composed of distinct pitches, are absolute universals that occur in all song traditions, say enthnomusicologist Patrick Savage of Tokyo University of the Arts and his colleagues. However, 18 features are statistical universals: They occur in a large majority of musical cultures, the researchers report June 29 in the Proceedings of the National Academy of Sciences.